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BRIEF COMMUNICATION: An update on genetic parameters for facial eczema tolerance in sheep

Abstract

Facial Eczema (FE) is a metabolic disease resulting
from liver and bile-duct damage, caused by ingestion of
the mycotoxin sporidesmin A, found in the spores of the
fungus Pithomyces chartarum. Risk of FE is associated
with temperature, humidity and dead leaf matter (Mitchell
et al. 1959; Brook 1963; Di Menna & Bailey 1973). While
FE is predominantly prevalent in the North Island of New
Zealand, climatic change projections indicate that there
will be an increase in the geographical spread of the fungus
and associated sporidesmin, resulting in FE spreading to
regions that are currently unaffected (Dennis et al. 2014).
Clinical FE is characterised by photosensitisation
due to liver injury; however, reduced production (Smith
2000) and reproduction (Moore et al. 1983; Mcmillan et al.
1988; Morris et al. 1991) is also observed in both clinically
and sub-clinically affected animals. The heritability of
liver damage at slaughter post-sporidesmin challenge was
estimated to be 0.42 ± 0.09 (Campbell et al. 1981). In the
live animal, serum gamma glutamyltransferase (GGT)
collected 2 to 3 weeks after sporidesmin challenge can
be used as a measure of liver damage (Towers & Stratton
1978). Romney FE selection lines, initially selected for
resistance or susceptibility on the basis of liver damage,
were established in 1975...

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